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在急性髓性白血病细胞中,ONC212通过触发SLC35F2表达和NOXA依赖的MCL1降解来增强YM155细胞毒性

Jing-Ting Chiou1, Long-Sen Chang2

  • 1Institute of Biomedical Sciences, National Sun Yat-Sen University, Kaohsiung 804, Taiwan.

Biochemical pharmacology
|April 28, 2024
PubMed
概括

在急性髓性白血病 (AML) 细胞中,ONC212通过AKT/NOX4/HuR/ATF4通路下调MCL1来诱导细胞亡. 这种机制增强了组合疗法的疗效,显示出显著的抗AML活性.

关键词:
急性骨髓性白血病 (AML) 是一种急性骨髓性白血病.在NOXA依赖的MCL1降解过程中,NOXA依赖的MCL1降解过程中.在ONC21212上,我们可以看到在SLC35F2F2中使用.对于YM155的协同性细胞毒性

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